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Biomedical subjects

T Kaji

Publications and source records attributed to T Kaji.

At least 109 records · Page 6Linked to original sources
PubMed1993

Zinc protection against cadmium-induced destruction of the monolayer of cultured vascular endothelial cells.

The effect of zinc on the destruction of vascular endothelial cell monolayer caused by cadmium was investigated using bovine aortic endothelial cells in a culture system. It was histologically revealed that cadmium-induced de-endothelialized area formation was markedly prevented by zinc. Zinc prevented cadmium-induced detachment of [3H]thymidine-labeled endothelial cells from the monolayer. Although cadmium increased the activity of lactate dehydrogenase in the medium, a marker of nonspecific cell damage, zinc markedly suppressed it. On the other hand, zinc significantly prevented cadmium-induced decrease in the incorporation of [3H]thymidine into the acid-insoluble fraction of the growing cells. From these results, it was suggested that impairment of the endothelial cell monolayer caused by cadmium is protected by zinc; this protection was postulated to be due to both a reduction of the cell detachment caused by cadmium-induced nonspecific cell damage and a decrease in cadmium inhibition of the cell proliferation which would help the repair of de-endothelialized areas.

Analysis of Variance↗
PubMed1993

Modulation by endothelin-1 of tissue plasminogen activator and plasminogen activator inhibitor-1 release from cultured human vascular endothelial cells: interaction of endothelin-1 with cytokines.

The interaction of endothelin-1 (ET-1) with either interleukin-1 beta (IL-1 beta) or tumor necrosis factor alpha (TNF alpha) on the release of tissue plasminogen activator antigen (t-PA:Ag) and plasminogen activator inhibitor-1 antigen (PAI-1:Ag) was investigated in a culture system of vascular endothelial cells derived from human umbilical vein. The t-PA:Ag release was significantly decreased by either IL-1 beta or TNF alpha; ET-1 intensified the suppressive effect of the cytokines. In contrast, PAI-1:Ag release was significantly increased by either IL-1 beta or TNF alpha; ET-1 significantly reduced the stimulatory effect of the cytokines. The data suggest that endothelial cell-mediated fibrinolysis may be modulated by ET-1.

Cells, Cultured↗
PubMed1993

Characterization of tumor necrosis factor alpha-induced alteration of glycosaminoglycans in cultured cells: comparison among vascular smooth-muscle cells, vascular endothelial cells, Chang liver cells and LLC-PK1 cells.

We investigated the alteration of glycosaminoglycans (GAGs) induced by recombinant human tumor necrosis factor alpha (rhTNF alpha) using confluent cultures of bovine aortic smooth-muscle cells, bovine aortic endothelial cells, Chang liver cells and porcine kidney LLC-PK1 cells. It was found that the incorporation of both [35S]sulfate and [3H]glucosamine into GAGs in the trypsinate fraction of the cell layer was significantly decreased by rhTNF alpha in vascular smooth-muscle cells and vascular endothelial cells; the incorporation of [35S]sulfate was increased but that of [3H]glucosamine was unchanged in Chang liver cells; the incorporation of both [35S]sulfate and [3H]glucosamine was increased by rhTNF alpha in LLC-PK1 cells. In the conditioned medium, the incorporation of both [35S]sulfate and [3H]glucosamine was not greatly changed by rhTNF alpha in all tested cell types. Characterization of GAGs revealed that each cell type uniquely altered its GAGs after rhTNF alpha treatment; the cytokine-induced alteration of each GAG component was not necessarily the same among different cell types. It was therefore concluded that rhTNF alpha-induced alteration of GAGs is dependent upon cell type.

Animals↗
PubMed1993

[A case of long-standing isolated traumatic tricuspid regurgitation with remarkably dilated right cardiac chambers and pancytopenia].

We report a rare case of tricuspid regurgitation due to nonpenetrating chest trauma 33 years previously. A 79-year-old man suffered a blunt trauma due to a piece of wood at work in 1958. He suffered multiple rib fractures on the right side and was admitted. Since then, he began having shortness of breath on exertion and was treated with medication. The patient was transferred to the Division of Cardiology, Hakodate National Hospital in 1984. A chest x-ray film revealed a marked cardiomegaly. Cardiac catheterization showed severe tricuspid regurgitation. Hepatomegaly and pancytopenia was observed. He was readmitted because of general fatigue in July 1991. Two-dimensional echocardiography demonstrated systolic excursion of septal and posterior tricuspid leaflets with ruptured chordae tendineae into the right atrium, and a remarkably enlarged right ventricule, right atrium and vena cava interior. Cardiac catheterization was performed. The right atrial pressure-wave form resembled the right ventricular pressure recording (ventricularization of the atrial pressure). Right ventricular cineangiography revealed severe tricuspid regurgitation, grade 4. Laboratory data showed pancytopenia. Thrombocytopenia progressed (3 x 10(4)/mm3), and a hemorrhagic tendency developed. The liver edge was palpable 4 finger breadths below the right costal margin. Pancytopenia due to congestive hepatomegaly and hypersplenism would have complicated this case.

Accidents, Occupational↗
PubMed1993

Emetic responses of Sorex unguiculatus.

We have shown previously that Suncus murinus, a species of the insectivore, can vomit in response to various emetogenic stimuli. In the present study we investigated whether or not Sorex unguiculatus, which belongs to different subfamily (Soricinae) of insectivore, vomits in response to emetogenic drugs. Subcutaneous injection of veratrine and oral administration of copper sulfate caused emesis in the animal. Histological study showed that bilateral structure of the area postrema was not important for the emetic reflex. Therefore, the capability of emesis may be common to the family of soricidae of the insectivore, and the Sorex unguiculatus is the smallest known mammal which can vomit.

Animals↗
PubMed1992

[CT of intestinal injuries following blunt trauma].

We retrospectively reviewed 53 CT scans in 42 patients with surgically proven intestinal injury following blunt abdominal trauma. Free air and localized low density fluid were specific signs of intestinal injury. Free peritoneal fluid without a known source, thickened bowel wall, and thickened mesentery were non-specific ones. Specific and non-specific findings were demonstrated in six (22%) and 23 (85%) of 27 CT scans performed within four hours following trauma, and 19 (73%) and 26 (100%) of 26 CT scans performed after four hours, respectively. CT is useful for the diagnosis of blunt intestinal injuries, but early diagnosis is difficult because of the lack of specific signs.

Abdominal Injuries↗
PubMed1992

Possible mechanism for zinc protection against cadmium cytotoxicity in cultured vascular endothelial cells.

We investigated the effect of zinc on cadmium cytotoxicity in vascular endothelial cells in a culture system. The cytotoxicity was evaluated by [3H]adenine release assay. Cadmium at 2 microM concentration and above significantly increased the [3H]adenine release, but zinc at 80 microM and below did not induce such a response after a 24-h incubation. Metallothionein was induced by cadmium at 0.1 microM and above but not by zinc at 300 microM and below; however, zinc at 10 microM and above significantly decreased cadmium-(2 and 5 microM) induced cytotoxicity. Zinc protection against cadmium cytotoxicity was also observed in the presence of 1 microM cycloheximide. Zinc caused significantly less accumulation of cadmium in the cell layer accompanied with a significant accumulation of zinc. The distribution (%) of cadmium in the particulate fraction of the cells was significantly decreased by zinc. In contrast, cadmium in the cytosol fraction was increased in the cells treated with both cadmium and zinc. Gel filtration chromatography of the cytosol showed that cadmium was capable of being bound to high-molecular-weight proteins and metallothionein. The metallothionein-bound cadmium was not increased by zinc; however, the relative distribution of cadmium in the high-molecular-weight fraction in the cytosol was decreased in cadmium plus zinc-treated cells. From these results, it was suggested that the mechanism by which zinc protects endothelial cells from cadmium cytotoxicity was decreased accumulation of cadmium in the particulate fraction and in the high-molecular-weight fraction in the cytosol of the cells. This alteration is postulated to be caused by both zinc-induced decrease in the intracellular cadmium accumulation and the sequestration of cadmium by cadmium-induced metallothionein.

Adenine↗
PubMed1992

Crystallization and preliminary X-ray study of the cathepsin B complexed with CA074, a selective inhibitor.

Cathepsin B from bovine spleen has been purified and crystallized as a complex with a specific inhibitor CA074 [N-(L-3-trans-propylcarbamoyloxirane-2-carbonyl)-L- isoleucyl-L-proline], using the hanging-drop method. The complex crystals obtained from 50 mM-citrate buffer (pH 3.5) belong to the tetragonal space group P4(1) (or P4(3)) with a = 73.06 A and c = 141.59 A, and diffract beyond 2.2 A resolution. There are two complex molecules per asymmetric unit giving a packing density of 3.37 A3/Da and indicating a high solvent content of 63.5%.

Animals↗
PubMed1992

[MR imaging of corpus callosal injuries].

The MR imaging and CT findings of corpus callosal injury were analyzed in 32 of 224 patients with acute head injuries. MR imaging was more sensitive than CT in the detection of callosal injuries. All 9 hemorrhagic lesions were visualized on both MR imaging and CT. Fifteen of 23 nonhemorrhagic lesions were not visualized on CT, although all nonhemorrhagic lesions were visualized on MR imaging. Twenty-four lesions of the corpus callosum were located in the splenium, but no lesion was located in the rostrum. Diffuse axonal shear injuries were visualized in 25 patients with callosal injury as associated traumatic lesions. Twenty-three patients with callosal injury had low initial Glasgow Coma Scale scores (less than 9), but 9 patients had high scores. Associated diffuse axonal shear injuries, especially in the brain stem could be a possible explanation for this difference. MR imaging is useful to detect traumatic lesions of the corpus callosum.

Accidents, Traffic↗
PubMed1992

[Evaluation of non-contrast-enhanced CT in blunt abdominal trauma].

We compared the findings of noncontrast-enhanced CT with those of contrast-enhanced CT in 126 patients with blunt abdominal trauma to evaluate the usefulness of noncontrast-enhanced CT. In 112 of the patients, visceral injuries were confirmed by surgery or clinical follow-up including CT. Although noncontrast-enhanced CT diagnosed all patients with 12 intestinal injuries requiring immediate surgery, contrast-enhanced CT missed two of these patients because high density hematomas on noncontrast-enhanced CT became isodense after IV administration of contrast material. However, contrast-enhanced CT was superior to noncontrast-enhanced CT in the diagnosis of hepatic and renal injuries. A case of renal artery occlusion was only visualized on contrast-enhanced CT. We conclude that both noncontrast- and contrast-enhanced CT should be performed for the CT evaluation of blunt abdominal trauma.

Abdominal Injuries↗
PubMed1992

Plasmin stimulates the release of dermatan sulfate from vascular smooth muscle cells in culture.

We investigated the effect of plasmin on the release of sulfated glycosaminoglycans (GAG) from cultured vascular smooth muscle cells. Confluent cultures of vascular smooth muscle cells from bovine aorta were labelled with [35S]sulfate and incubated at 37 degrees C for principally 60 min in a serum-free medium in the presence of plasmin. Plasmin at 10 mU/ml (approximately 2.7 micrograms/ml) and above significantly increased the release of [35S]sulfate-labeled GAG (35S-GAG) from the cell layer after a 60 min incubation. A time course study showed that plasmin at 10 mU/ml significantly increased the 35S-GAG release after 20 min and longer. However, plasminogen at 100 mU/ml and below did not cause a significant change of the 35S-GAG release after a 90 min incubation. A characterization of 35S-GAG revealed that plasmin increased both dermatan sulfate and the other 35S-GAG in the medium. Plasmin at 100 mU/ml enhanced the cell detachment significantly but only slightly. From these results, it was suggested that a endogenous thrombin inhibitor heparin cofactor II may be activated in the liquid phase by dermatan sulfate released from plasmin-stimulated vascular smooth muscle cells when the vascular is disrupted and plasma is exposed to extravessel.

Animals↗
PubMed1992

Effect of cadmium on the monolayer maintenance of vascular endothelial cells in culture.

We investigated the effect of cadmium on the maintenance of the monolayer of vascular endothelial cells to clarify a possible involvement of endothelium injury in cadmium-induced vascular disorders. Endothelial cells from bovine aorta were cultured with cadmium chloride (0.5, 1.0, 2.0 or 5.0 microM) for 24 or 72 h. A histological observation revealed that a de-endothelialized space was formed in the monolayer by cadmium treatment; the number of endothelial cells was significantly decreased by the metal. Cadmium significantly decreased the number of growing endothelial cells with a significant decrease in the [3H]thymidine incorporation, suggesting that cadmium inhibited the cell proliferation. On the other hand, cadmium significantly increased the detachment of [3H]thymidine-labeled endothelial cells from the monolayer with a parallel increase in the lactate dehydrogenase activity in the medium. From these results, it was suggested that cadmium impairs the endothelial cell monolayer; the de-endothelialized space was formed by both an increase in the cell detachment by cadmium cytotoxicity and a retardation of the repair of the space which was due to an inhibition of the cell proliferation caused by the metal.

Animals↗
PubMed1992

Inhibitory effect of lead on the release of tissue plasminogen activator from human vascular endothelial cells in culture.

To evaluate the toxicity of lead on the blood fibrinolytic system, vascular endothelial cells from human umbilical vein were cultured in the presence of lead and the content of tissue plasminogen activator antigen (t-PA:Ag) released into the medium was determined by enzyme immunoassay. It was found that lead significantly decreased the t-PA:Ag release from the cells. Although heavy metals including cadmium, mercury, cobalt, manganese, nickel, zinc and copper as well as lead each had an inhibitory effect, lead was the potent inhibitor. Lead significantly disturbed thrombin up-regulation of t-PA:Ag release and significantly amplified endothelin-1 down-regulation of it. Incorporation of [3H]thymidine into the acid-insoluble fraction of the cell layer was significantly increased by lead; however, that of [14C]leucine was unchanged by the metal. In lead-treated cells, a significant accumulation of lead was observed but calcium content was increased slightly. From these results, it was suggested that lead decreased the release of t-PA:Ag from cultured endothelial cells without nonspecific inhibition of protein synthesis; lead may stimulate the calcium-dependent down-regulation of endothelial cell t-PA:Ag release by calcium or by mimicking calcium.

Calcium↗
PubMed1992

Reversibility of the inhibitory effect of rhodamine B on the proliferation of cultured human lip fibroblasts.

To investigate the reversibility of rhodamine B inhibition of cell proliferation, human lip fibroblast KD cells were cultured for 3 days in the presence of 25 or 50 micrograms/ml of the dye and the effect of removal of the dye from the culture medium on cell histology and on incorporation of [3H]thymidine into the acid-insoluble fraction of the cell layer was investigated. Removal of rhodamine B on the last 1 or 2 days resulted in an increase in cell number, and incorporation of [3H]thymidine was also restored after removal of the dye; [3H]thymidine incorporation by the cells treated with the dye for only the 1st day was the same as that by the control cells cultured without the dye. In conclusion, it was shown that the decrease in KD cell proliferation caused by rhodamine B can be reversed by removal of the dye.

Cell Division↗